|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Zoology, La Trobe University, Bundoora, Victoria, Australia
* To whom correspondence should be addressed. E-mail: t.dutka{at}latrobe.edu.au.
The Na+-K+ pumps in the transverse tubular (T-) system of a muscle fiber play a vital role keeping [K+] in the T-system sufficiently low during activity so as to prevent chronic depolarization and consequent loss of excitability. These Na+-K+ pumps are located in the triad junction, the key transduction zone controlling excitation-contraction (EC-) coupling, a region rich in glycolytic enzymes and likely having high localised ATP usage and limited substrate diffusion. This study examined whether Na+-K+ pump function was dependent on ATP derived via the glycolytic pathway locally within the triad region. Single fibers from rat fast-twitch muscle were mechanically skinned, sealing off the T-system but retaining normal EC-coupling. Intracellular composition was set by the bathing solution, and action potentials (APs) triggered in the T-system, eliciting intracellular Ca2+ release and twitch and tetanic force responses. Conditions were selected such that increased Na+-K+ pump function could be detected from the consequent increase in T-system polarization and resultant faster rate of AP repriming. Na+-K+ pump function was not adequately supported by maintaining cytoplasmic [ATP] at its normal resting level (~8 mM), even with 10 mM or 40 mM creatine phosphate (CP) present. Addition of as little as 1 mM of phospho(enol)pyruvate (PEP) resulted in a marked increase in Na+-K+ pump function, supported by endogenous pyruvate kinase (PK) bound within the triad. These results demonstrate that the triad junction is a highly restricted micro-environment, where glycolytic re-synthesis of ATP is critical to meet high demand of the Na+-K+ pump and maintain muscle excitability.
This article has been cited by other articles:
![]() |
G. A. Ramirez-Correa, W. Jin, Z. Wang, X. Zhong, W. D. Gao, W. B. Dias, C. Vecoli, G. W. Hart, and A. M. Murphy O-Linked GlcNAc Modification of Cardiac Myofilament Proteins: A Novel Regulator of Myocardial Contractile Function Circ. Res., December 5, 2008; 103(12): 1354 - 1358. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. P. Cairns and M. I. Lindinger Do multiple ionic interactions contribute to skeletal muscle fatigue? J. Physiol., September 1, 2008; 586(17): 4039 - 4054. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Nordsborg, J. Ovesen, M. Thomassen, M. Zangenberg, C. Jons, F. M. Iaia, J. J. Nielsen, and J. Bangsbo Effect of dexamethasone on skeletal muscle Na+,K+ pump subunit specific expression and K+ homeostasis during exercise in humans J. Physiol., March 1, 2008; 586(5): 1447 - 1459. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. L. Dutka, R. M. Murphy, D. G. Stephenson, and G. D. Lamb Chloride conductance in the transverse tubular system of rat skeletal muscle fibres: importance in excitation-contraction coupling and fatigue J. Physiol., February 1, 2008; 586(3): 875 - 887. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. G. Allen, G. D. Lamb, and H. Westerblad Skeletal Muscle Fatigue: Cellular Mechanisms Physiol Rev, January 1, 2008; 88(1): 287 - 332. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |